Associate Professor of Medicine
Harvard Medical School
Division of Immunology
Dr. Kaur's laboratory is conducting research on AIDS pathogenesis in nonhuman
primates infected with the simian immunodeficiency virus (SIV). Research projects include
investigation of the immunopathogenesis of cytomegalovirus (CMV) and other herpesvirus
infections in simian AIDS, host responses in natural hosts of SIV that do not develop AIDS, and
determinants of protective immunity induced by AIDS vaccines.
CMV immunopathogenesis: CMV is an important opportunistic infection associated with an
increased risk of progression to AIDS. The rhesus macaque model of simian AIDS is being used
to investigate the immune basis of CMV reactivation in AIDS. The components of cellular
immunity involved in resolution of primary viremia and maintenance of asymptomatic, latent
infection are being investigated in immunocompetent and SIV-infected macaques. Studies
involving in vivo depletion of T cell subsets, and phenotypic and functional examination of
CMV-specific T cells, are being used to understand mechanisms of impairment of
immunological memory in AIDS.
Host responses to SIV in sooty mangabeys: Sooty mangabeys are a natural host of SIV that
typically do not progress to AIDS despite the presence of persistent, high-level viremia.
Research is focused on analyzing the role of SIV-specific cellular immune responses and innate
immunity in maintaining non-pathogenic SIV infection in sooty mangabeys.
AIDS Vaccine: Recombinant herpes simplex virus vector-based AIDS vaccines are being
tested for protective efficacy in rhesus macaques. Determinants of protective immunity
including functional and phenotypic properties of memory T cells, and induction of mucosal
immunity are being investigated.
Kaur A, Hale CL, Ramanujan S, Jain RK, Johnson RP.
Differential dynamics of CD4+ and CD8+ T lymphocyte proliferation and activation in acute
simian immunodeficiency virus infection. J. Virol. 2000; 74:8413-8424.
Kaur A, Hale Cl, Noren B, Kassis N, Simon MA, Johnson RP. Decreased frequency of cytomegalovirus-specific CD4+ T lymphocytes in SIV-infected rhesus macaques: inverse relationship with CMV viremia. J. Virol. 2002; 76:
Kaur A, Kassis N, Hale Cl, Simon MA, Elliott M,
Gomez-Yafal A, Lifson JD, Desrosiers RC, Wang F, Barry P, Mach M, Johnson RP. Direct
relationship between suppression of virus-specific immunity and emergence of cytomegalovirus
disease in simian AIDS. J. Virol. 2003; 77:5749-5758.
Kaur A, Sanford HB, Garry D, Lang S, Klumpp SA, Watanabe D, Bronson RT, Lifson JD,
Rosati M, Pavlakis GN, Felber BK, Knipe DM, Desrosiers RC. Ability of herpes simplex virus vectors to boost
immune responses of DNA vectors and to protect against challenge by simian Immunodeficiency virus. Virology. 2007; 357:
A, Di Mascio M, Barabasz A, Rosenzweig M, McClure HM, Perelson AS, Ribeiro RM, Johnson RP. Dynamics of T and B lymphocyte turnover in a
natural host of a simian immunodeficiency virus. J Virology, in press.
Yue Y, Kaur A, Eberhardt MK, Kassis N, Zhou SS, Tarantal AF, Barry PA. Immunogenicity and protective efficacy of DNA vaccines expressing rhesus cytomegalovirus glycoprotein B, phosphoprotein 65-2, and viral interleuking-10 in rhesus macaques J. Virol. 2007; 81: 1095-1109.
Chan K, Kaur A. Flow cytometric detection of degranulation reveals phenotypic heterogeneity of degranulation CMV-specific CD8+ T lymphocytes in rhesus macaques. J. Immunol. 2007; 325: 20-34.
Wang, Z, Metcalf, B, Ribeiro, RM, McClure, H, Kaur, A.
Th-1 type cytotoxic CD8+ T lymphocyte responses to simian immunodeficiency virus (SIV) are
a consistent feature of natural SIV infection in sooty mangabeys. J. Virol. 2006;
Fogg, MH, Garry, D, Awad A, Wang
F, Kaur A. The BZLF1 homolog of an Epstein-Barr-related γ-herpesvirus is a frequent
target of the CTL response in persistently infected rhesus macaques. J. Immunol. 2006 Mar 15;176(6):3391-401.